Electrostimulation of catecholamine release in the eel: modulation by antagonists and autocrine agonists.
The innervated chromaffin cells of the eel (Anguilla rostrata) release norepinephrine (NE) and epinephrine (E), while a component of the macrovascular wall releases dopamine (DA). The release of the three catecholamines is governed by complex controls which include adrenergic, nicotinergic, muscarinergic, and opioid mechanisms. To gain insight into the interactions between neural and autocrine factors in stimulated catecholamine release, we investigated the effect of adrenergic (phentolamine and propranolol) and muscarinergic (atropine) receptor antagonists, and of autocrine opioids (met-enkephalin, codeine, and morphine) on electrostimulated catecholamine secretion in situ. The hind brain (close to the root of nerve IX) of anesthetized eels was stimulated at four different time points, and segments of the posterior cardinal vein or the caudal vein were perfused with a saline solution, with or without test substances. Electrostimulation (30 s) four times within a total study duration of 14 min increased the release of DA, NE, and E into the perfusate of the cardinal vein. The vessel contains the innervated adrenomedullary equivalent. In the noninnervated caudal vein electrical stimulation had no impact on total DA release, while there was a slight decrease of NE release and a slight increase of E release. In the cardinal vein, both the alpha-adrenergic receptor antagonist phentolamine and the beta-adrenergic receptor antagonist propranolol strongly reduced the effect of electrostimulation on catecholamine release. Met-enkephalin reduced the release of all three catecholamines to a similar degree; its impact on NE release was especially strong. Codeine reduced the catecholamine release moderately, while morphine had no effect. Atropine reduced the release of all three catecholamines in a pattern similar to that of met-enkephalin. The findings on the posterior cardinal vein indicate that neurally stimulated NE and E release (1) involves autocrine/paracrine adrenergic mechanisms, (2) involves a muscarinergic mechanism, and possibly also endogenous codeine and morphine; and (3) is antagonized by met-enkephalin. The findings on the caudal vein are further evidence that macrovascular DA release is not under direct neural control.
Abele
B
B
Department of Pathology, Anatomy, and Cell Biology, Thomas Jefferson University, Philadelphia, Pennsylvania 19107, USA.
Hathaway
C B
CB
Nibbio
B
B
Epple
A
A
D000322:Adrenergic Agonists / Q000494:pharmacology*; D018674:Adrenergic Antagonists / Q000494:pharmacology*; D000811:Anguilla / Q000502:physiology*; D000818:Animals; D019898:Autocrine Communication / Q000187:drug effects*; D002395:Catecholamines / Q000819:agonists / Q000037:antagonists & inhibitors / Q000378:metabolism*; D004298:Dopamine / Q000378:metabolism; D004558:Electric Stimulation; D004744:Enkephalin, Methionine / Q000494:pharmacology; D004837:Epinephrine; D018721:Muscarinic Agonists / Q000494:pharmacology; D009638:Norepinephrine / Q000378:metabolism; D011941:Receptors, Adrenergic / Q000187:drug effects
D000322:Adrenergic Agonists; D018674:Adrenergic Antagonists; D002395:Catecholamines; D018721:Muscarinic Agonists; D011941:Receptors, Adrenergic; D004744:Enkephalin, Methionine; D004298:Dopamine; D009638:Norepinephrine; D004837:Epinephrine